In vivo, rehmapicroside suppressed 3-nitrotyrosine formation, Drp1 nitration as well as NADPH oxidases and iNOS expression in the ischemia-reperfused rat brains; it also prevented the translocations of PINK1, Parkin, and Drp1 into the mitochondria for mitophagy activation; finally, rehmapicroside ameliorated infarct sizes and improved neurological deficit scores in the rats with transient MCAO cerebral ischemia. Here, FMO5 is linked to ischemia.